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![Heart failure -- Epidemiology
Prevalence • > 2% - 3% overall; 10% - 20% at > 70 yrs
• European society of cardiology countries : > 15
milion patients with heart failure and increasing
Burden • Primary cause of 5% of hospital admissions
• Present in 10% of hospitalized patients
• 2% of national health expenditure [60% - 70% of cost
due to heart failure hospitalization]
• 40% of patients admitted to hospital with heart
failure are dead or readmitted within 1 yr
Mcmurray J J Et Al Eur Heart J 2013; 33 [14]: 1787-1847
Dickstein K Et Al Eur Heart J 2006; 29: 2388-2442
FinalPathwaysDisease](https://image.slidesharecdn.com/heartfailureapi2014-160204104127/85/Heart-failure-api-2-320.jpg)
![Linking Short- term intervention with long-term benefit:
What is needed?
Better understanding of Acute Heart Failure pathophysiology
MORTALITY
• Myocardial injury [Tn
release]
• Renal dysfunction [CRS]
• Liver dysfunction
PREVENTION OF END-
ORGAN DAMAGE
Congestion
Viable but
dysfunctional
myocardium
Neurohormonal
& inflammatory
activation
Mechanisms which
can be targeted
Metabolic
factors
Hemodynamic
deterioration
[↑LVFP,↓ CO, ↓ PERFUSION]
Vascular resistance
/stiffness ↑
ESC guidelines for the diagnosis and treatment of acute and chronic heart failure 2012 Reviewed by Ponikowski](https://image.slidesharecdn.com/heartfailureapi2014-160204104127/85/Heart-failure-api-9-320.jpg)
![Cumulative benefits of medical therapy on mortality. Adapted, with permission, from Fonarow GC, et al.
Potential impact of optimal implementation of evidence-based heart failure therapies on mortality. Am
Heart J 2011;161:1024-30.
Heart Failure Therapies
Beta-blocker
Beta-blocker +
ACEI/ARB
Beta-blocker +
ACEI/ARB+ ICD
Beta-blocker +
ACEI/ARB+ ICD+
HF education
Beta-blocker +
ACEI/ARB+ ICD+
HF education+
anticoagulation for
AF
Beta-blocker +
ACEI/ARB+ ICD+
HF education+
anticoagulation
for AF +CRT
ChangeinOddsof24-MonthMortality(%)
-39%
[-28% to -49%]
P < 0.0001
-63%
[-54% to -71%]
P < 0.0001 -76%
[-68% to -81%]
P < 0.0001
-81%
[-75% to -86%]
P < 0.0001
-83%
[-77% to -88%]
P < 0.0001
-81%
[-72% to -87%]
P < 0.0001](https://image.slidesharecdn.com/heartfailureapi2014-160204104127/85/Heart-failure-api-24-320.jpg)
![Number needed to treat for mortality
25
Guideline
recommended
therapy
Relative risk
reduction in
mortality
Number needed
to treat for
mortality
Number
needed to treat
for mortality
[ standardized
to 36 mths]
Relative risk
reduction in HF
hospitalisations
ACEI / ARB 17% 22 over 42 mths 26 31%
Beta blocker 34% 28 over 12 mths 9 41%
Aldosterone
antagonist
30% 9 over 24 months 6 35%
Hydralazine /
nitrate
43% 25 over 10 mths 7 33%
CRT 36% 12 over 24 mths 8 52%
ICD 23% 14 over 60 mths 23 NA
Reproduced with permission from Fonarow GC et al Am Heart j 2011; 161: 1024-30](https://image.slidesharecdn.com/heartfailureapi2014-160204104127/85/Heart-failure-api-25-320.jpg)
More Related Content
Heart failure api
- 1. Prof. U. C.SAMAL MD, FICC, FACC, FIACM, FIAE, FISE, FISC, FAPVS Ex- Prof. Cardiology & Ex-HOD Medicine Patna Medical College, Patna, Bihar Past President, Indian College of Cardiology Permanent & Chief Trustee, ICC-Heart Failure Foundation National Convener Heart Failure Sub Specialty, CSI Executive Member (National), Cardiological Society of India President, CSI Bihar / Vice President, API Bihar 1 HEART FAILURE
- 2. Heart failure --Epidemiology Prevalence • > 2% - 3% overall; 10% - 20% at > 70 yrs • European society of cardiology countries : > 15 milion patients with heart failure and increasing Burden • Primary cause of 5% of hospital admissions • Present in 10% of hospitalized patients • 2% of national health expenditure [60% - 70% of cost due to heart failure hospitalization] • 40% of patients admitted to hospital with heart failure are dead or readmitted within 1 yr Mcmurray J J Et Al Eur Heart J 2013; 33 [14]: 1787-1847 Dickstein K Et Al Eur Heart J 2006; 29: 2388-2442 FinalPathwaysDisease
- 3. Total Population ofIndia - 1.16 Billion (2009 Est)
- 4. Classification of HeartFailure ACCF/AHA Stages of HF NYHA Functional Classification A At high risk for HF but without structural heart disease or symptoms of HF. None B Structural heart disease but without signs or symptoms of HF. I No limitation of physical activity. Ordinary physical activity does not cause symptoms of HF. C Structural heart disease with prior or current symptoms of HF. I No limitation of physical activity. Ordinary physical activity does not cause symptoms of HF. II Slight limitation of physical activity. Comfortable at rest, but ordinary physical activity results in symptoms of HF. III Marked limitation of physical activity. Comfortable at rest, but less than ordinary activity causes symptoms of HF. IV Unable to carry on any physical activity without symptoms of HF, or symptoms of HF at rest. D Refractory HF requiring specialized interventions.
- 5. Stages, Phenotypes andTreatment of HF 2013 ACCF/AHA Guideline for the Management of Heart Failure
- 7. • diuretics • ultrafiltration Vasodilators •nitroglycerin • nesiritide • nitroprusside INOTROPES • dobutamine • dopamine • levosimendan • nitroprusside Fluid retention or redistribution ? Pulmoedema?? “dry out” “warm up & “dry out” Assessment of hemodynamic profile : therapeutic implications Adapted from Stevenson L W, Eur Heart j 7 SIGNS/SYMPTOMS CONGESTION: DYSPNOEA/( EXERTION /REST) ORTHOPNEA PNH JV DISTENSION RALES (uncommon in chronic cases) LOUD P2 INCREASING S3 PEDAL OEDEMA ABDOMINOJUGULAR REFLUX ASCITES VALSALVA SQUARE WAVE POSSIBLE EVIDENCE OF LOW PERFUSION: SLEEPY / OBTUNDED COOL EXTREMITIES NARROW PULSE PRESSURE HYPOTENSION WITH ACE INHIBITOR LOW SERUM SODIUM AKI / RENAL DYSFUNCTION ELEVATED LFTs PULSUS ALTERNANS 67% 28%5% 67% 28%5% ACE-I / ARB/ BB/ MRA MM/ MN
- 9. Linking Short- termintervention with long-term benefit: What is needed? Better understanding of Acute Heart Failure pathophysiology MORTALITY • Myocardial injury [Tn release] • Renal dysfunction [CRS] • Liver dysfunction PREVENTION OF END- ORGAN DAMAGE Congestion Viable but dysfunctional myocardium Neurohormonal & inflammatory activation Mechanisms which can be targeted Metabolic factors Hemodynamic deterioration [↑LVFP,↓ CO, ↓ PERFUSION] Vascular resistance /stiffness ↑ ESC guidelines for the diagnosis and treatment of acute and chronic heart failure 2012 Reviewed by Ponikowski
- 10. Diagnosis of HFin untreated patients with symptoms suggestive of HF using natriuretic peptides Clinical examination ECG, Chest X-ray Echocardiography Natriuretic peptides BNP < 100pg/ml NT-proBNP < 400pg/ml BNP < 100-400 pg/ml NT-proBNP 400-2000 pg/ml BNP > 400 pg/ml NT-proBNP > 2000 pg/ml Chronic HF likely Uncertain diagnosis Chronic HF likely
- 11. “HF management ‘guided’by natriuretic peptides would be superior to standard HF therapy alone.” 11 van Kimmenade, R. R. & Januzzi, J. L. Jr. Clin. Chem. 58, 127–138 (2012).
- 12. 12 Clinical Value ofdiagnostic testing modality : BNP/ NT-BNP Adapted and reprinted with permission from Januzzi JL,Camargo CA, Anwarudding S ,et al. The N-terminal Pro- BNP investigation of Dyspnea in the Emergency Department (PRIDE) Study. Am J Cardiol 2005;95:948-954
- 13. Effect of cardiacand extra cardiac parameters on BNP and NT-proBNP Raised in Cardiac Factors Lower Ejection Fraction, Larger Left ventricular mass, Atrial size, Atrial fibrillation, Coronary heart disease , Valvular heart disease, Acute coronary syndrome, Cor pulmonale (acute/ chronic), COLD (right heart strain) Extra Cardiac factors Age, Female gender, Low glomerular filtration, Hematocrit low, Hyperthyroidism, Cushing syndrome. Liver cirrhosis with ascites, paraneoplastic syndrome, Subarachnoidal bleeding, Sepsis, Rheumatic diseases, Stroke Reduced in Extra Cardiac factors Obesity,ACE-I/ARB, Diuretics, Hypothyroidsm, Primary hyperaldosteronism Biomarkers in medicine 3.5 (Oct 2009) p465 13
- 14. 14 “For example, overthe past 2 decades, the once-held view of chronic HF as a syndrome of disordered hemodynamics and fluid balance caused by alterations in the structure of the heart has been succeeded by a view of the disease that involves molecular pathways in disarray. Chronic HF is now seen as a systemic illness that involves interplay between myocardial factors, systemic inflammation, renal dysfunction, and neurohormonal activation. Our assessment and treatment of patients with chronic HF has, thus, progressed from a focus on improving hemodynamics to measuring and modifying the maladaptive molecular processes that contribute to progression of disease” Braunwald, E. N. Engl. J. Med. 358, 2148–2159 (2008).
- 15. Neurohormones Norepinephrine Renin Angiotensin II Copeptin Endothelin Vascular system Homocysteine Adhesionmolecules (ICAM, P-selectin) Endothelin Adiponectin C-type natriuretic peptide Inflammation C-reactive protein sST2 Tumor necrosis factor FAS (APO-1) GDF-15 Pentraxin 3 Adipokines Cytokines Procalcitonin Osteoprotegerin Myocardial stress Natriuretic peptides Mid-regional pro-adrenomedullin Neuregulin sST2 Myocardial injury Cardiac troponins High sensitivity cardiac troponins Myosin light-chain kinase 1 Heart-type fatty acid binding protein Pentraxin 3 Matrix and cellular remodeling Galectin-3 sST2 GDF-15 MMPs TIMPs Collagen propeptides Osteopontin Cardio-renal syndrome Creatinine Cystatin C NGAL ß-Trace protein Oxidative stress Oxidized LDL Myeloperoxidase Urinary biopyrrins Urinary and plasma isoprostanes Plasma malondialdehyde HF as a systemic illness. 15 Nature Review Cardiology Vol.9 June 12 pg 349
- 16. “HF-CBS-SRS” Quantitative results in~15 minutes! EDTA Whole Blood , No Centrifugation Anywhere, anytime, in time Point of Care System for rapid, accurate results • Easy • Portable • Reliable Results in about minutes Fluorescence Sandwich immunoassay Test Normal Range CKMB ng/mL (0.0 - 4.3) MYO ng/mL (0.0 – 107) TNI ng/mL (0.00 - 0.40) BNP pg/mL (0.00 - 100) DDIM ng/mL (0.0 - 400) NGAL* ng/mL (0-149) PANEL OF SOB TRIAGE/ AMI/ AKI 15 6 Biomarkers 750 +750 bucks * Galectin3/BNP+NGAL being uploaded to the test platform 16
- 17. SOB TRIAGE METER PLATFORM ParametersNormal Range Cost(Rs.) Timing CKMB 0.0-4.3 SOB PANEL Rs. 750 10-15 Min MYO 0.0-107 TNI 0.00-0.40 BNP 0.00-100 DDIM 0.1-400 NAGAL 0-149 Rs. 850 15 Min
- 18. Triage® Meter: ThreeSimple Steps 1. Add whole blood to Test Device 2. Insert Test Device into Meter 3. Read results
- 19. Intelligent Nephelometry Technology SmartCard Calibration Economic 10 Parameter Assay Panel ser- friendly 3 Step Assay Procedure No Sample dilution Test Normal Range ASO I/mL (50 - 1000) CRP mg/L (0.5 - 320) RF I/mL (10-120) HbA1c % (3-13%) IgE I/mL (1-1000) MICROALBMIN mg/L (5-200) Lp(a) Mg/dl (1-100) CYSTATIN C mg/L (0.0-10) FERRITIN I/mL (1-1000) D-DIMER ng/mL REPORT OF MISPA PANEL SERUM / URINE “HF-CBS-SRS” Measures ACR & Routine rine Parameters • 95% Correlation with conventional immunoturbidimetric test • Analyze spot rine sample • Works on batteries or power cable • Provides Printed report “15/23 Minutes Exercise” 10 Biomarkers 1000 Bucks 19
- 20. Agappe Mispa carries ISO13485:2003 and CE marking; GMP and FDA compliant ISO 9001: 2008 certified
- 21.
- 22. Parameters Pack sizeTest Range Normal Range Price Timing ASO 30 Test 50-1000 IU/ml 0-200 IU/ml 62 5 Min CRP 30 Test 0.5-250 mg/L 0.000-6.000mg/L 51 5Min RF 30 TEST 10-120 IU/ml 0.000-20.000/IU/ml 46 6 min CYSTATIN C 30 TEST 0.1-10 mg/L 0.000-1.149 mg/L 161 6 min HbA1C 30 TEST 3-13% 4.000-6.000 % 160 7 min D-DIMER 30 TEST 0-400 ng/mL 0.000-400 ng/ml 160 7 min IgE 30 TEST 0-1000 IU/mL 0.000-400 IU/mL 180 6 min FERRITIN 30 TEST 0-1000 ng/mL 0.000-230 ng/mL 200 6 min Lp(a) 30 TEST 1-100 mg/dL 0-30 mg/dL 180 7 min MICROALBUMIN 30 TEST 5-200 mg/L 0.000-25.000 mg/L 101 5 min Intelligent Double Chanel Nephlometry Technology
- 23. Possible future strategiesfor biomarker-guided therapies in chronic HF. 2013-14 Optimism : Ahmad T et al Nat. Rev. Cardiol.9,347-359(2012) 23
- 24. Cumulative benefits ofmedical therapy on mortality. Adapted, with permission, from Fonarow GC, et al. Potential impact of optimal implementation of evidence-based heart failure therapies on mortality. Am Heart J 2011;161:1024-30. Heart Failure Therapies Beta-blocker Beta-blocker + ACEI/ARB Beta-blocker + ACEI/ARB+ ICD Beta-blocker + ACEI/ARB+ ICD+ HF education Beta-blocker + ACEI/ARB+ ICD+ HF education+ anticoagulation for AF Beta-blocker + ACEI/ARB+ ICD+ HF education+ anticoagulation for AF +CRT ChangeinOddsof24-MonthMortality(%) -39% [-28% to -49%] P < 0.0001 -63% [-54% to -71%] P < 0.0001 -76% [-68% to -81%] P < 0.0001 -81% [-75% to -86%] P < 0.0001 -83% [-77% to -88%] P < 0.0001 -81% [-72% to -87%] P < 0.0001
- 25. Number needed totreat for mortality 25 Guideline recommended therapy Relative risk reduction in mortality Number needed to treat for mortality Number needed to treat for mortality [ standardized to 36 mths] Relative risk reduction in HF hospitalisations ACEI / ARB 17% 22 over 42 mths 26 31% Beta blocker 34% 28 over 12 mths 9 41% Aldosterone antagonist 30% 9 over 24 months 6 35% Hydralazine / nitrate 43% 25 over 10 mths 7 33% CRT 36% 12 over 24 mths 8 52% ICD 23% 14 over 60 mths 23 NA Reproduced with permission from Fonarow GC et al Am Heart j 2011; 161: 1024-30
- 26. Milton Packer 2008JCF • … Yet, despite substantial advances in our understanding and management of heart failure, we have had • few successes and many failures. • Nearly 1,000 new drugs and devices have been developed for the treatment of heart failure duringthe past 20 years, but only 9 have received regulatory approval and are being used in the clinical setting. • Most of our efforts to correct fluid retention, stimulate the inotropic state of the heart, and modulate neurohormonal systems have not predictably improved the condition of patients with HF…
- 27. “Poly Client Challenge” •Poly co-morbidities • Poly – pharmacy • Poly - side effects • Poly – healthcare providers • Poly - clinics • Poly-labs / investigation • POLY – CONFUSION……. END RESULT You must have patience to find little pink hope!!! Yes , a Pandora’s box ! but Heart Failure Care is always rewarding
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- 30.
- 31. HF---- We are allequals but some are better equals Heart Failurists are less equal
- 32.
- 33.
Editor's Notes
- #16 HF as a systemic illness. HF involves interplay between myocardial factors, systemic inflammation, renal dysfunction, and neurohormonal activation. Biomarkers can be classified according to broad categories of processes that are involved in the development and progression of chronic HF. Several biomarkers have been characterized for each of these processes; these vary greatly in their ease of measurement, cost, turnaround time, and evaluation in the clinical setting. Traditional biomarkers that have been studied fairly rigorously appear in italics. Abbreviations: APO, apoptosis antigen; GDF, growth-differentiation factor; HF, heart failure; ICAM, intercellular adhesion molecule; MMPs, matrix metalloproteinases; NGAL, neutrophil gelatinase-associated lipocalin; TIMPs, matrix metalloproteinase tissue inhibitors.